Julia Darzi

How effective are current dietary guidelines for cardiovascular disease prevention in healthy middle-aged and older men and women? A randomized controlled trial

BACKGROUND Controversy surrounds the effectiveness of dietary guidelines for cardiovascular disease (CVD) prevention in healthy middle-aged and older men and women. OBJECTIVE The objective was to compare effects on vascular and lipid CVD risk factors of following the United Kingdom dietary guidelines with a traditional British diet (control). DESIGN With the use of a parallel-designed randomized controlled trial in 165 healthy nonsmoking men and women (aged 40-70 y), we measured ambulatory blood pressure (BP) on 5 occasions, vascular function, and CVD risk factors at baseline and during 12 wk after random assignment to treatment. The primary outcomes were differences between treatments in daytime ambulatory systolic BP, flow-mediated dilation, and total cholesterol/HDL cholesterol. Secondary outcomes were differences between treatment in carotid-to-femoral pulse wave velocity, high-sensitivity C-reactive protein, and a measure of insulin sensitivity (Revised Quantitative Insulin Sensitivity Check Index). RESULTS Data were available on 162 participants, and adherence to the dietary advice was confirmed from dietary records and biomarkers of compliance. In the dietary guidelines group (n = 80) compared with control (n = 82), daytime systolic BP was 4.2 mm Hg (95% CI: 1.7, 6.6 mm Hg; P < 0.001) lower, the treatment effect on flow-mediated dilation [-0.62% (95% CI: -1.48%, 0.24%)] was not significant, the total cholesterol:HDL cholesterol ratio was 0.13 (95% CI: 0, 0.26; P = 0.044) lower, pulse wave velocity was 0.29 m/s (95% CI: 0.07, 0.52 m/s; P = 0.011) lower, high-sensitivity C-reactive protein was 36% (95% CI: 7%, 48%; P = 0.017) lower, the treatment effect on the Revised Quantitative Insulin Sensitivity Check Index [2% (95% CI: -2%, 5%)] was not significant, and body weight was 1.9 kg (95% CI: 1.3, 2.5 kg; P < 0.001) lower. Causal mediated effects analysis based on urinary sodium excretion indicated that sodium reduction explained 2.4 mm Hg (95% CI: 1.0, 3.9 mm Hg) of the fall in blood pressure. CONCLUSION Selecting a diet consistent with current dietary guidelines lowers BP and lipids, which would be expected to reduce the risk of CVD by one-third in healthy middle-aged and older men and women. This study is registered at www.isrctn.com as 92382106.

The effects of partial sleep deprivation on energy balance: A systematic review and meta-analysis

Background/Objectives:It is unknown whether short sleep duration causatively contributes to weight gain. Studies investigating effects of partial sleep deprivation (PSD) on energy balance components report conflicting findings. Our objective was to conduct a systematic review and meta-analysis of human intervention studies assessing the effects of PSD on energy intake (EI) and energy expenditure (EE).Subjects/Methods:EMBASE, Medline, Cochrane CENTRAL, Web of Science and Scopus were searched. Differences in EI and total EE following PSD compared with a control condition were generated using the inverse variance method with random-effects models. Secondary outcomes included macronutrient distribution and resting metabolic rate. Heterogeneity was quantified with the I2-statistic.Results:Seventeen studies (n=496) were eligible for inclusion in the systematic review, and 11 studies (n=172) provided sufficient data to be included in meta-analyses. EI was significantly increased by 385 kcal (95% confidence interval: 252, 517; P<0.00001) following PSD compared with the control condition. We found no significant change in total EE or resting metabolic rate as a result of PSD. The observed increase in EI was accompanied by significantly higher fat and lower protein intakes, but no effect on carbohydrate intake.Conclusions:The pooled effects of the studies with extractable data indicated that PSD resulted in increased EI with no effect on EE, leading to a net positive energy balance, which in the long term may contribute to weight gain.

Influence of the tolerability of vinegar as an oral source of short-chain fatty acids on appetite control and food intake

Background:Vinegar is promoted as a natural appetite suppressant, based on previous reports that vinegar ingestion significantly increases subsequent satiety. However there are concerns about the appropriateness and safety of this advice, and it is unclear if poor product palatability may explain previously published effects on appetite.Objective:To investigate if vinegar palatability and tolerability have a role in suppressing appetite and food intake in two sequential and related acute human feeding studies.Subjects and methods:Healthy, young, normal weight unrestrained eaters were recruited to Study 1 (n=16), an acute feeding study supplying vinegar within both palatable and unpalatable drinks alongside a mixed breakfast in comparison to a non-vinegar control; and to Study 2 (n=14), a modified sham feeding study (taste only without ingestion) comparing vinegar to a non-vinegar control following a milkshake preload. Both studies were a randomized crossover balanced design for the assessment of appetite, energy intake and glycaemic response.Results:In Study 1, ingestion of vinegar significantly reduced quantitative and subjective measures of appetite, which were accompanied by significantly higher nausea ratings, with unpalatable treatment having the greatest effect. Significant correlations between palatability ratings and appetite measures were found. In Study 2, orosensory stimulation with vinegar did not influence subsequent subjective or quantitative measures of appetite compared with control.Conclusions:These studies indicate that vinegar ingestion enhances satiety whereas orosensory stimulation alone does not, and that these effects are largely due to poor tolerability following ingestion invoking feelings of nausea. On this basis the promotion of vinegar as a natural appetite suppressant does not seem appropriate.

Sleep extension is a feasible lifestyle intervention in free-living adults who are habitually short sleepers: a potential strategy for decreasing intake of free sugars? A randomized controlled pilot study

ABSTRACT Background Evidence suggests that short sleep duration may be a newly identified modifiable risk factor for obesity, yet there is a paucity of studies to investigate this. Objective We assessed the feasibility of a personalized sleep extension protocol in adults aged 18–64 y who are habitually short sleepers (5 to <7 h), with sleep primarily measured by wrist actigraphy. In addition, we collected pilot data to assess the effects of extended sleep on dietary intake and quality measured by 7-d food diaries, resting and total energy expenditure, physical activity, and markers of cardiometabolic health. Design Forty-two normal-weight healthy participants who were habitually short sleepers completed this free-living, 4-wk, parallel-design randomized controlled trial. The sleep extension group (n = 21) received a behavioral consultation session targeting sleep hygiene. The control group (n = 21) maintained habitual short sleep. Results Rates of participation, attrition, and compliance were 100%, 6.5%, and 85.7%, respectively. The sleep extension group significantly increased time in bed [0:55 hours:minutes (h:mm); 95% CI: 0:37, 1:12 h:mm], sleep period (0:47 h:mm; 95% CI: 0:29, 1:05 h:mm), and sleep duration (0:21 h:mm; 95% CI: 0:06, 0:36 h:mm) compared with the control group. Sleep extension led to reduced intake of free sugars (–9.6 g; 95% CI: –16.0, –3.1 g) compared with control (0.7 g; 95% CI: –5.7, 7.2 g) (P = 0.042). A sensitivity analysis in plausible reporters showed that the sleep extension group reduced intakes of fat (percentage), carbohydrates (grams), and free sugars (grams) in comparison to the control group. There were no significant differences between groups in markers of energy balance or cardiometabolic health. Conclusions We showed the feasibility of extending sleep in adult short sleepers. Sleep extension led to reduced free sugar intakes and may be a viable strategy to facilitate limiting excessive consumption of free sugars in an obesity-promoting environment. This trial was registered at www.clinicaltrials.gov as NCT02787577.

l-rhamnose as a source of colonic propionate inhibits insulin secretion but does not influence measures of appetite or food intake

Activation of free fatty acid receptor (FFAR)2 and FFAR3 via colonic short-chain fatty acids, particularly propionate, are postulated to explain observed inverse associations between dietary fiber intake and body weight. Propionate is reported as the predominant colonic fermentation product from l-rhamnose, a natural monosaccharide that resists digestion and absorption reaching the colon intact, while effects of long-chain inulin on appetite have not been extensively investigated. In this single-blind randomized crossover study, healthy unrestrained eaters (n = 13) ingested 25.5 g/d l-rhamnose, 22.4 g/d inulin or no supplement (control) alongside a standardized breakfast and lunch, following a 6-d run-in to investigate if appetite was inhibited. Postprandial qualitative appetite, breath hydrogen, and plasma glucose, insulin, triglycerides and non-esterified fatty acids were assessed for 420 min, then an ad libitum meal was provided. Significant treatment x time effects were found for postprandial insulin (P = 0.009) and non-esterified fatty acids (P = 0.046) with a significantly lower insulin response for l-rhamnose (P = 0.023) than control. No differences between treatments were found for quantitative and qualitative appetite measures, although significant treatment x time effects for meal desire (P = 0.008) and desire to eat sweet (P = 0.036) were found. Breath hydrogen was significantly higher with inulin (P = 0.001) and l-rhamnose (P = 0.009) than control, indicating colonic fermentation. These findings suggest l-rhamnose may inhibit postprandial insulin secretion, however neither l-rhamnose or inulin influenced appetite.

The feasibility of lengthening sleep in habitually short sleepers and its effect on dietary intake, energy balance, and metabolic risk factors: A randomised controlled trial

H.K. Al Khatib, W.L. Hall, A. Creedon, E. Ooi, T. Masri, S.V. Harding, L. McGowan, J. Darzi* and G.K. Pot* Diabetes & Nutritional Sciences Division, Faculty of Life Sciences & Medicine, King’s College London, London SE1 9NH, U.K., Centre for Public Health, School of Medicine, Dentistry and Biomedical Sciences, Queens University Belfast, Belfast BT12 6BA, U.K. and Department of Health and Life, Virje Universiteit Amsterdam, Faculty of Earth and Life Sciences, Amsterdam, The Netherlands

Be nutrition aware in primary care: making every contact count

The role of nutritional status and dietary intake in influencing health and disease cannot be overstated, impacting at all stages of the life cycle. There is unequivocal evidence that risk of non-communicable disease, including cardiovascular disease, the leading cause of death in the UK, is strongly associated with obesity, nutritional status, and diet quality. As such, diet and lifestyle advice are important components in the management of many chronic diseases and disorders. Less well recognised is the role of protein-energy undernutrition (referred to as malnutrition herein) in negatively impacting on disease risk, progression, and prognosis. As the first point of contact for most people accessing health care is via primary care, GPs are in a good position to identify and manage those patients who would benefit from nutritional care. This editorial will focus specifically on the ‘dual burden’ of obesity and malnutrition, although there are many other areas of health and disease in which nutrition is also fundamental. Proper nutritional care has been highlighted by the Royal College of Physicians as a core area of responsibility for doctors in the care of their patients.1 Key recommendations include that doctors should encourage patients to avoid becoming, and treat those who are, overweight; doctors should have a key role in the detection and management of malnutrition; and that nutritional screening should be integral to clinical practice. Despite this, there are concerns that nutrition …